Chemoreceptors central

Compare and contrast the function of the peripheral and central chemoreceptors... 

The central chemoreceptors are located near the ventral surface of the medulla in close proximity to the respiratory center. These receptors are surrounded by the extracellular fluid (ECF) of the brain and respond to changes in H+ ion concentration. The composition of the ECF surrounding the central chemoreceptors is determined by the cerebrospinal fluid (CSF), local blood flow, and local metabolism. 

A summary of the responses of the peripheral and the central chemoreceptors to reduced arterial oxygen, increased arterial carbon dioxide, and increased arterial hydrogen ion concentration is found in Table 17.2. 

Chemoreceptor response to decreased arterial P02. Hypoxia has a direct depressant effect on central chemoreceptors as well as on the medullary respiratory center. In fact, hypoxia tends to inhibit activity in all regions of the brain. Therefore, the ventilatory response to hypoxemia is elicited only by the peripheral chemoreceptors. 

An increase in arterial PC02 results in marked stimulation of the central chemoreceptors. In fact, this is the most important factor in regulation of ventilation. It is well known that it is impossible to hold one s breath indefinitely. As carbon dioxide accumulates in the arterial blood, the excitatory input to the respiratory center from the central chemoreceptors overrides the voluntary inhibitory input and breathing resumes. Furthermore, this occurs well before the arterial P02 falls low enough to stimulate the peripheral chemoreceptors. 

Carbonic anhydrase (CA) facilitates the formation of carbonic acid (H2C03) from carbon dioxide and water. The carbonic acid then dissociates to liberate hydrogen ion (H+) and bicarbonate ion (HC03-). The hydrogen ions strongly stimulate the central chemoreceptors to increase ventilation. The ensuing elimination of excess carbon dioxide from the arterial blood returns the PC02 to its normal value. 

Conversely, a decrease in the arterial PCOz due to hyperventilation results in a decrease in the H+ ion concentration in the ECF of the brain. Decreased stimulation of the central chemoreceptors (and therefore a decrease in the excitatory input to the medullary respiratory center) causes... 

Chemoreceptor response to increased arterial hydrogen ion concentration. An increase in arterial hydrogen ion concentration, or a decrease in arterial pH, stimulates the peripheral chemoreceptors and enhances ventilation. This response is important in maintaining acid-base balance. For example, under conditions of metabolic acidosis, caused by the accumulation of acids in the blood, the enhanced ventilation eliminates carbon dioxide and thus reduces the concentration of H+ ions in the blood. Metabolic acidosis may occur in patients with uncontrolled diabetes mellitus or when tissues become hypoxic and produce lactic acid. An increase in arterial hydrogen ion concentration has no effect on the central chemoreceptors. Hydrogen ions are unable to cross the blood-brain barrier. 

Q6 The respiratory system compensates for alkalosis by retaining C02. The central chemoreceptors in the medullary respiratory centres respond to the reduced H+ by decreasing alveolar ventilation, which will increase blood arterial PC02 and return the pH to normal (7.4). 

Chemoreceptors sense concentrations of oxygen, carbon, and carbon dioxide in the blood. A change in concentration causes the chemoreceptors to send a message to the central chemoreceptors located in the medulla. The medulla then sends the necessary physiological response through cerebrospinal fluid. 

Most metabolic acid-base disorders develop slowly, within hours in diabetic ketoacidosis and months or even years in chronic renal disease. The respiratory system responds immediately to a change in acid-base status, but several hours maybe required for the response to become maximal. The maximum response is not attained until both the central and peripheral chemoreceptors are fully stimulated. For example, in the early stages of metabolic acidosis, plasma pH decreases, but because H ions equilibrate rather slowly across the blood-brain barrier, the pH in CSF remains nearly normal. However, because peripheral chemoreceptors are stimulated by the decreased plasma pH, hyperventilation occurs, and plasma PCO2 decreases. When this occurs, the PCO2 of the CSF decreases immediately because CO2 equilibrates rapidly across the blood-brain barrier, leading to a rise in the pH of the CSF. This will inhibit the central chemoreceptors. But as plasma bicarbonate gradually falls because of acidosis, bicarbonate concentration and pH in the CSF wih also fall over several hours. At this point, stimulation of respiration becomes maximal as both the central and peripheral chemoreceptors are maximally stimulated. 

The reverse is true when a patient with metabolic acidosis is treated with HCOT When the pH in plasma increases as the result of HCOj administration, stimulation of the peripheral chemoreceptors returns to normal. However, because of the slow equilibration of HCOj between plasma and CSF, the central chemoreceptors continue to be stimulated, and the patient continues to hyperventilate, even when the blood pH has returned to normal. Respiration does not return to normal until normal acid-base balance in the CSF of the brain is restored. 

Abstract CO2 and H are metabolic end-products, which are produced continuously and excreted steadily to maintain steady-state concentrations of CO2/H+ in the body, primarily by the chemoreceptors. To help maintain an adequate speed of reaction compatible with life, these reactions are enhanced by carbonic anhydrase (CA) present in the chemoreceptor cells. The role of chemoreceptors in H homeostasis is the focus of this chapter. The peripheral chemoreceptors very readily sense CO2/H and stimulate ventilation in order to enhance CO2 exhalation. Central chemoreceptors are stimulated similarly but slowly, also resulting in increased ventilation. Altogether, this phase, assisted by respiration alone, can be defined as the acute response. However, the H left behind is excreted by the renal system, rather slowly (chronic phase) without any direct intervention by the chemoreceptors. Thus, respiratory and renal systems are integrated in the long run to maintain ( XT/H homeostasis. 

There are two sets of sensors peripheral and central chemoreceptors. The peripheral receptors reside in the... 

In addition, central chemoreceptor will also respond by increasing ventilation, which will be followed by corrective renal response. These general considerations are given in detail elsewhere (Lahiri and Forster, 2003). 

ATP is released extracellularly in the ventrolateral medulla during hypercapnia because of activation of central chemoreceptors. The action of hypercapnia is on P2 receptors localized in close proximity to the VLM inspiratory neurons. But the cellular sources of ATP released are yet to be investigated (Spyer and Thomas, 2000 Spyer et al., 2004, Gourine, 2005). 

When the effect of PaO2 is lost, although the PaCO, effect is normal, it is due primarily to central chemoreceptor stimulation. The indications are that the stimulation due to carotid chemoreceptor is minimal (Milledge and Lahiri, 1967). 

Regardless of the actual mechanism or precise location of the central chemoreceptors, these chemosensitive areas have the following important functional characteristics related to respiratory regulation ... 

Increases in arterial pco2 result in central chemoreceptor stimulation mainly through the rapid diffusion of C02 into the CSF and the associated increase in [H+] from the acidification of C02 with water. 

Central chemoreceptors respond more slowly to pco2 and [H+] changes in arterial blood than do the peripheral receptors. 

In general, the principal function of the central chemoreceptors is to guard the [H+] of CSF which bathes the central nervous system while the principal function of the peripheral chemoreceptors is to regulate po2 and, under extreme conditions, the pco2 and [H+] of systemic arterial blood (25). 

During the period in which Horgan and Lange were carrying on their studies, Clegg (37) presented a careful study of respiratory control which followed a more basic control approach than that used previously. The schematic representation of the system is shown in Figure 4. This work, which is seldom referenced, represented one of the first attempts at specifying the relative importance of the peripheral and central chemoreceptors to respiratory dynamics and stability. The model exhibited realistic transient and steady-state behavior under various conditions. 

A. Mechanism of action. Ipecac causes vomiting In two phases by direct irritation of the gastric mucosa and by systemic absorption and stimulation of the central chemoreceptor trigger zone. 

The two major peripheral chemoreceptors are the carotid and the aortic bodies. The central chemoreceptors are probably localized close to the respiratory center in the medulla. 

The central chemoreceptor normally has a greater sensitivity than the peripheral chemoreceptors (which may be silenced by hyperoxia). Their combined effects are presumably additive at... 

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